Abstract
It has been shown that MHV-4 (JHM) can utilize both endosomal and nonendosomal pathways for entry into cells, depending on the strain of the virus and the nature of the cell being infected (Nash and Buchmeier, 1997). Wildtype MHV-4 fuses at the cell surface. However, persistent MHV-4 infection of a neuronal cell line (OBL21a) gave rise to the acid-dependent fusion variant OBLV60. Previous studies demonstrated that there were 8 amino acid differences between the S genes of MHV-4 and OBLV60. Elimination of neutral pH fusion was dependent only on amino acid alterations at positions 1067 (Q to H), 1094 (Q to H), and 1114 (L to R) within the first heptad repeat of the S2 subunit (Gallagher et al, 1991). Additionally, it was shown that intranasal inoculation with MHV-4 resulted in fatal encephalitis as a consequence of widespread distribution of infection in the brain. In contrast, the OBLV60 variant grew preferentially in the glomerular and mitral layers of the olfactory bulb and no fatal encephalitis was observed (Pearce et al., 1994).
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De Groot, L., Piñón, J.D., Phillips, J., Lavi, E., Weiss, S.R. (2001). Pathogenesis of Fusion Deficient Recombinant Mouse Hepatitis Viruses. In: Lavi, E., Weiss, S.R., Hingley, S.T. (eds) The Nidoviruses. Advances in Experimental Medicine and Biology, vol 494. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1325-4_26
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DOI: https://doi.org/10.1007/978-1-4615-1325-4_26
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